ArticleCancer management and research2025
Activating Transcription Factor 5 Promotes Tumorigenic Capability in Cervical Cancer Through the Wnt/β-Catenin Signaling Pathway.
Article in Cancer management and research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- MiR-4725-3p acts as an oncogene and prognostic biomarker in hepatocellular carcinoma.World journal of surgical oncology · 2026Article
- The potential of ATF5 as a prognostic marker and therapeutic target in cancer: insights from bioinformatics analysis and experimental validation.Translational cancer research · 2026Article
- Unleashing Wnts: Wnt Ligands Fuel Cancer Spread.Journal of cancer biology · 2025Article
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4 authors.
Funding
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Abstract
Purpose: Cervical cancer is the fourth leading cause of cancer-related death in women. Furthermore, owing to its significant risk of recurrence or metastasis, the overall prognosis of patients with cervical cancer remains poor. Activating transcription factor 5 (ATF5) plays a crucial role in cell proliferation, survival, and apoptosis, and has been implicated in the progression of various types of cancer. However, the biological function and precise mechanism of ATF5 in cervical cancer remain unclear. This study, aimed to explore the function of ATF5 and its potential mechanisms in cervical cancer. Patients and Methods: Quantitative real-time PCR, Western blot and immunohistochemistry were used to detect the expression of ATF5 in cervical cancer tissues and cell lines. Knockdown ATF5 expression in cervical cancer cell lines was constructed using lentivirus-mediated shRNA to explore the role of ATF5 in cervical cancer through cell viability, transwell, and wound healing experiments. The expression of Wnt3a and β-catenin were investigated using quantitative real-time PCR and Western blot. Results: ATF5 was overexpressed in cervical cancer, and upregulation of ATF5 expression was associated with a poor prognosis. ATF5 knockdown inhibited the proliferation, migration and invasion abilities of cervical cancer cells. Furthermore, the downregulation of ATF5 led to the suppression of Wnt3a and β-catenin expression, which are key molecules in the Wnt/β-catenin signaling pathway. Conclusion: ATF5 promotes tumorigenic capability in cervical cancer through the Wnt/β-catenin signaling pathway. ATF5 may be a potential prognostic biomarker and therapeutic target in the management of cervical cancer.
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